论文部分内容阅读
目的 :系统观察新分离呼肠病毒感染食蟹猴的病理学变化 ,探讨其发病机制。方法 :用从SARS患者分离的呼肠病毒BYD1株通过滴鼻和静脉注射两种途径 ,感染 4只食蟹猴 (每组 2只 )。每组分别在感染后 7d和 33d各处死 1只 ,进行肺脏、心肌、肝脏、脾脏、肾脏、肠、脑和淋巴等组织病理学检查。结果 :肉眼观察感染猴肺组织可见水肿和红白相间的实变。病理组织学变化主要集中在肺脏、脾脏、淋巴结和全身小静脉。肺脏表现局部肺泡腔出血 ,并有蛋白液渗出。肺泡间隔充血、淤血、水肿 ,导致肺泡壁增厚。支气管上皮细胞和黏膜纤毛脱落 ,支气管周围单核细胞浸润。脾脏、淋巴结白髓减少 ,红髓淤血 ,发生中心淋巴细胞数量减少。全身组织器官小静脉明显淤血。结论 :食蟹猴实验感染呼肠病毒BYD1株后 ,出现间质性肺炎 ,脾脏、淋巴结萎缩和全身小静脉淤血等一系列组织病理学特征。病毒感染后 ,受侵害肺脏出现血氧交换障碍和免疫器官功能下降是导致食蟹猴发病的内在机制。新分离的呼肠病毒感染食蟹猴出现的病理学变化提示可以作为严重呼吸综合征的病理学模型。
Objective: To systematically observe the pathological changes of newly isolated reovirus-infected cynomolgus monkeys and to explore its pathogenesis. Methods: Four cynomolgus monkeys (two per group) were infected by both intranasal and intravenous routes with reovirus BYD1 strain isolated from SARS patients. Each group was sacrificed at 7d and 33d after infection, respectively. Histopathological examination was performed on the lung, myocardium, liver, spleen, kidney, intestine, brain and lymph. Results: Macroscopic observation of infected monkey lung tissue edema and red and white consolidation. Histopathological changes mainly in the lungs, spleen, lymph nodes and systemic veins. Local lung alveolar hemorrhage showed performance, and protein exudation. Alveolar septum congestion, congestion, edema, leading to alveolar wall thickening. Bronchial epithelial cells and mucociliary shedding, infiltration of peripheral mononuclear cells. Spleen, lymph node white pulp reduction, congestion of the red pulp, the occurrence of central lymphocytes decreased. Systemic organs and small veins obviously congestion. Conclusion: Cynomolgus monkeys infected with BYD1 strain of reovirus showed a series of histopathological features such as interstitial pneumonia, spleen, lymph node atrophy and systemic venous congestion. After the virus infection, impaired lung oxygen exchange disorders and immune function decline is the leading mechanism of cynomolgus pathogenesis. Pathological changes in newly isolated reovirus-infected cynomolgus monkeys suggest that they may serve as a pathological model of severe respiratory syndrome.